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Increased number of CD4-CD8+ MHC class II-specific T cells in MHC class II-deficient mice.

机译:MHC II类缺陷小鼠中CD4-CD8 + MHC II类特异性T细胞数量增加。

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摘要

Targeted disruption of the A beta-encoding gene of H2b mice abolishes major histocompatibility complex (MHC) class II expression and results in a failure to develop CD4+8- T cells. Besides this major effect, the lack of class II expression affects the level of T-cell receptor (TCR) and CD4 expression on differentiating thymocytes. Moreover, there is no class II-mediated negative selection of thymocytes. All this could result in TCR repertoire changes of the CD4-8+ T-cell subpopulation, which apparently develops normally in these mice. To test this hypothesis, the class II reactivity of CD4-8+ T cells from class II-deficient (class II0) mice was analysed. It was found that CD4-8+ T cells from class II0 but not from class II-expressing mice developed a significant level of cytotoxicity against class II-expressing target cells. These results demonstrate an influence of MHC class II molecules on the TCR repertoire of CD4-8+ T cells.
机译:H2b小鼠的Aβ编码基因的靶向破坏取消了主要的组织相容性复合物(MHC)II类表达,并导致无法发育CD4 + 8- T细胞。除此主要作用外,缺乏II类表达会影响分化胸腺细胞上T细胞受体(TCR)和CD4表达的水平。而且,没有II类介导的胸腺细胞阴性选择。所有这些都可能导致CD4-8 + T细胞亚群的TCR库变化,这些变化显然在这些小鼠中正常发生。为了检验该假设,分析了来自II类缺陷(II0类)小鼠的CD4-8 + T细胞的II类反应性。已经发现,来自II0类而不是来自表达II类的小鼠的CD4-8 + T细胞对表达II类的靶细胞产生了显着水平的细胞毒性。这些结果证明II类MHC分子对CD4-8 + T细胞的TCR库有影响。

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